The physiology and pharmacology of the activation and inhibition of the electrogenic sodium pump were investigated in the sympathetic ganglia of bullfrogs, using the sucrose gap technique. The administration of nicotinic cholinergic agonists produces a brief depolarization that is followed by an after-hyperpolarization that is due to activation of the electrogenic sodium pump. This electrogenic pumping of sodium was rapidly inhibited by potassium-free Ringer. The after-hyperpolarization was also inhibited after one hour in ouabain (1 uM). Potassium-free Ringer resulted in an accumulation of intracellular sodium ions, so that normal Ringer's solution produced a hyperpolarization of the membrane due to activation of the electrogenic sodium pump. This hyperpolarization was inhibited after one hour in ouabain (1 uM). These results indicate that the electrogenic sodium pump can be activated in two ways: (1) following a nicotinic cholinergic depolarization; and (2) by return from potassium-free to normal Ringer's solution. Furthermore, the electrogenic sodium pump can be inhibited by potassium-free Ringer and by ouabain.